Abnormal FUS protein aggregates have been observed in several neurodegenerative diseases, including ALS, FTLD, and polyglutamine disease [30], FUS aggregation in ALS appears at the early stages of the disease, contributing well to the disease pathogenesis [32] Compared to SOD1 or TDP-43 mutation carriers, FUS mutation carriers have shown a slightly younger age of disease onset and their survival time appeared to be shorter [33]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.